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脑促生长素对正常及链脲佐菌素诱导的糖尿病大鼠淋巴细胞增殖转化活性的影响。

Effect of cerebrocrast on the lymphocyte blast transformation activity in normal and streptozotocin-induced diabetic rats.

作者信息

Briede J, Daija D, Stivrina M, Duburs G

机构信息

Latvian Institute of Organic Synthesis, Riga, Latvia.

出版信息

Cell Biochem Funct. 1999 Jun;17(2):89-96. doi: 10.1002/(SICI)1099-0844(199906)17:2<89::AID-CBF813>3.0.CO;2-2.

Abstract

Both IDDM and NIDDM are characterized by deviations in peripheral T and B lymphocyte count, Thelper: Tsuppressor ratio, as well as by impaired Tsuppressor function. These abnormalities may promote insulin antibody and other antibody production, contributing to overt diabetes mellitus development in early stage of the disease. In the present study we explored the effects of cerebrocrast(1, 4-dihydropyridine derivative) administration on Con A- and IL-2-stimulated tissue lymphocyte blast transformation activity and on the thymus and lymph node mass in normal and streptozotocin (STZ)-induced diabetic rats. It was established that cerebrocrast, administered four times at the doses of 0.05 and 0.5 mg kg-1, has long-term (up to 14 days) effects on the immune system and protects against the toxic effect of STZ in STZ-induced diabetic rats, preventing thymus and lymph node mass loss. We conclude that cerebrocrast administration leads to the increase in number and activity of Thelper and Tsuppressor lymphocytes. Glycolysis and DNA synthesis in these cells is augmented under the influence of cerebrocrast administration. We propose that the increase in lymphocyte suppressive activity caused by cerebrocrast administration may prevent the development of IDDM and NIDDM in patients with pre-diabetes, but in patients with early and overt diabetes mellitus the drug administration may prevent the overexpression of insulin antibodies and other antibodies. The effect of cerebrocrast on the de novo production of insulin and IL-2 receptors may be beneficial for IDDM and NIDDM patients.

摘要

胰岛素依赖型糖尿病(IDDM)和非胰岛素依赖型糖尿病(NIDDM)的特征均为外周T和B淋巴细胞计数、辅助性T细胞与抑制性T细胞比例出现偏差,以及抑制性T细胞功能受损。这些异常情况可能会促进胰岛素抗体和其他抗体的产生,从而在疾病早期导致明显的糖尿病发展。在本研究中,我们探讨了给予脑康宁(一种1,4 - 二氢吡啶衍生物)对正常大鼠和链脲佐菌素(STZ)诱导的糖尿病大鼠中,伴刀豆球蛋白A(Con A)和白细胞介素 - 2(IL - 2)刺激的组织淋巴细胞增殖转化活性以及胸腺和淋巴结质量的影响。已证实,以0.05和0.5 mg kg⁻¹的剂量给予脑康宁四次,对免疫系统具有长期(长达14天)影响,并能保护STZ诱导的糖尿病大鼠免受STZ的毒性作用,防止胸腺和淋巴结质量损失。我们得出结论,给予脑康宁会导致辅助性T细胞和抑制性T细胞数量及活性增加。在脑康宁的影响下,这些细胞中的糖酵解和DNA合成增强。我们提出,脑康宁给药引起的淋巴细胞抑制活性增加可能会预防糖尿病前期患者发生IDDM和NIDDM,但对于早期和明显糖尿病患者,给药可能会防止胰岛素抗体和其他抗体的过度表达。脑康宁对胰岛素和IL - 2受体从头产生的影响可能对IDDM和NIDDM患者有益。

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